Infection with herps simplex type 1 induces expression of receptors for C3b on mammalian cells previously devoid of such receptors. We have shown that the isolated glycoprotein responsible for this activity (gC) is a potent modulator of complement-mediated cytolysis in vitro, acting by at least two mechanisms. We have also aided in the demonstration of relative complement resistance by cells infected with wild type HSV-1, as opposed to cells infected with gC-defective mutant strains. Future plans include direct binding studies of purified C3 fragments to HSV-1 gC and defined fragments thereof, as well as cells infected with other human herpesviruses. The role of gC as a blocker of infected cell interactions with cytotoxic lymphocytes will also be studied.